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首页> 外文期刊>Archives of pharmacal research >The role of the endothelium in the regulation of vascular smooth muscle cell contractions induced by angiotensin II after ischemia and reperfusion.
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The role of the endothelium in the regulation of vascular smooth muscle cell contractions induced by angiotensin II after ischemia and reperfusion.

机译:内皮在调节缺血再灌注后血管紧张素Ⅱ诱导的血管平滑肌细胞收缩中的作用。

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In this study, we investigated smooth muscle cell contractions induced by angiotensin II (ANG II) in blood vessels with or without endothelium after ischemia/reperfusion. Experiments were done on tail arteries, with or without endothelium, of perfused male Wistar rats. We analyzed the influence of ANG II on vascular contractions in the presence of sodium nitroprusside or 8Br-cGMP and after ischemia/reperfusion using classical pharmacometric methods. Vascular contractions induced by ANG II were decreased by sodium nitroprusside and 8BrcGMP. Reductions in maximal response and increases in EC(50) values after ischemia were observed only in vessels with endothelium. After reperfusion, increases in maximal response and decreases in EC(50) values were observed. Decreases in ANG II induced vascular contractions on caused by ischemia involves the presence of endothelium, synthesis of nitric oxide and activation of cGMP. The increase in the reaction to ANG II that is induced by reperfusion is independent of the endothelium.
机译:在这项研究中,我们调查了血管紧张素II(ANG II)在缺血/再灌注后有或没有内皮的血管中诱导的平滑肌细胞收缩。在灌注的雄性Wistar大鼠的有或没有内皮的尾动脉上进行了实验。我们使用经典药理学方法分析了在硝普钠或8Br-cGMP存在下以及缺血/再灌注后ANG II对血管收缩的影响。硝普钠和8BrcGMP降低了ANG II诱导的血管收缩。仅在具有内皮的血管中观察到缺血后最大反应的降低和EC(50)值的增加。再灌注后,观察到最大反应增加,EC(50)值降低。由局部缺血引起的ANG II诱导的血管收缩的减少涉及内皮的存在,一氧化氮的合成和cGMP的激活。由再灌注诱导的对ANG II的反应的增加与内皮无关。

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